A weak heart can cause a suffering brain

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In a new study, researchers found that heart problems cause disturbed gene activity in the brain’s memory center, from which cognitive deficits arise.

They found a possible cause for the increased risk of dementia in people with heart problems.

Moreover, a specific drug that is known to affect gene activity may alleviate mental deficits.

The research was conducted by a team at the German Center for Neurodegenerative Diseases (DZNE) and elsewhere.

In Germany, about four million people are affected by heart failure: Their heart muscle is too weak to pump enough blood through the body and is therefore abnormally enlarged.

Physical fitness and quality of life suffer as a result. Moreover, affected people have an increased risk of developing dementia.

In the study, the team found in mice that impaired gene activity developed in the hippocampus as a result of heart problems.

In memory tests, mice with heart failure performed significantly worse than their healthy mates.

They then examined the neurons of the hippocampus. In the mice with heart failure, they found increased cellular stress pathways and altered gene activity in neurons.

The researchers are also investigating drugs. In previous studies, they were able to show that the cancer drug vorinostat can alleviate genetically driven as well as age-related memory problems in mice.

In this study, the scientists treated mice with heart failure with this drug. They found that the heart’s pumping capacity did not change significantly, but memory performance improved.

Currently, vorinostat is being investigated for the therapy of people with Alzheimer’s in a clinical trial.

The team says people with heart problems and heart failure, in particular, may experience noticeable cognitive deficits and an increased risk of developing Alzheimer’s disease.

Possible reasons include impaired blood supply to the brain and dysfunction of the hippocampus, which is the memory’s control center.

One author of the study is Prof. André Fischer, the research group leader.

The study is published in EMBO Molecular Medicine.

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